Pharmacology of Metformin—Its Molecular Mechanisms Underlying Versatile Cellular Responses

Dear Colleagues,

In the seventeenth century, herbal medicine with Galega officinalis (containing a guanidine compound that was used later as a template for metformin) was originally applied to the treatments for infectious disease with fever, including malaria infection, influenza outbreak, and snake bites. In some of the influenza patients, lowering blood glucose was observed as a beneficial side effect.

Nowadays, diverse effects of metformin (Met) against diabetes, cardiovascular diseases, cancers, cognitive decline, and ageing are widely appreciated. Met activates and promotes the proliferation of tumor-infiltrating CD8T lymphocytes (CD8TILs) while stimulating macrophage polarization into the M1-like phenotype and decreasing T regulatory cells (Treg) in the tumor microenvironment. On the other hand, Met prevents SARS-CoV-2-induced-lung damage via downregulating cytokine storm response. Met reduces inflammation by promoting the polarization of M2-like macrophages, Treg, and CD8 memory T cells. Met also attenuates autoimmune diseases, graft-versus-host disease.

In spite of the accumulation of evidence for such beneficial effect of Met, the underlying mechanisms are not fully understood. The social demands for the dissection of the detailed mechanisms have become higher than ever. In view of such events, this Special Issue, entitled “Pharmacology of Metformin—Its Molecular Mechanisms Underlying Versatile Cellular Responses”, specifically covers, but is not limited to, molecular mechanisms for the blood-glucose-lowering effect, cancer prevention, immunity, and longevity. For example, molecular mechanisms underlying preventions of cardiovascular diseases and neurodegeneration are welcome. Please be advised that molecular mechanism analysis would be encouraged but mere phenomenological theory or details of phenomena are not subject of adoption.

Prof. Dr. Heiichiro Udono
Guest Editor

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